Eosinophil Accumulation In Lung Research Articles

128 Oncostatin M-receptor Deficient Phenotype Provides Evidence that Oncostatin M is Critical for IL-4-induced Eosinophil Accumulation in Lungs In Vivo

128 Oncostatin M-receptor Deficient Phenotype Provides Evidence that Oncostatin M is Critical for IL-4-induced Eosinophil Accumulation in Lungs In Vivo

Liriopis tuber inhibit OVA-induced airway inflammation and bronchial hyperresponsiveness in murine model of asthma

Liriope platyphylla is one of the well-known herb used in oriental medicine for treatment asthma and bronchial and lung inflammation. Anti-asthmatic effects of Liriope platyphylla in the development of OVA-induced airway inflammation and murine asthma model have not been fully investigated in vivo. Asthma is a chronic inflammatory disease of the mucosa and is associated with excess production of Th2 cytokines and eosinophil accumulation in lung. To clarify the anti-inflammatory and anti-asthmatic effects of Liriope platyphylla, we examined the influence of liriopis tuber (LRT) on the development of pulmonary eosinophilic inflammation in murine model of asthma. Our results have shown that LRT were demonstrated on the accumulation of eosinophills into airways, with reduction of eosinophil, total lung leukocytes numbers by reduction IL-5, IL-13, IL-4 and IgE levels in the BALF and serum. Moreover, LRT decreased eosinophil CCR3 expression and CD11b expression in lung cells. These results indicate that LRT has a deep inhibitory effects on airway inflammation and hyperresponsiveness in murine model of asthma and play an crucial role as a immunomodulator which possess anti-inflammatory and anti-asthmatic property by modulating the relationship between Th1/Th2 cytokine imbalance.

Elemental signals regulating eosinophil accumulation in the lung.

In this review we identify the elemental signals that regulate eosinophil accumulation in the allergic lung. We show that there are two interwoven mechanisms for the accumulation of eosinophils in pulmonary tissues and that these mechanisms are linked to the development of airways hyperreactivity (AHR). Interleukin-(IL)-5 plays a critical role in the expansion of eosinophil pools in both the bone marrow and blood in response to allergen provocation of the airways. Secondly, IL-4 and IL-13 operate within the allergic lung to control the transmigration of eosinophils across the vascular bed into pulmonary tissues. This process exclusively promotes tissue accumulation of eosinophils. IL-13 and IL-4 probably act by activating eosinophil-specific adhesion pathways and by regulating the production of IL-5 and eotaxin in the lung compartment. IL-5 and eotaxin co-operate locally in pulmonary tissues to selectively and synergistically promote eosinophilia. Thus, IL-5 acts systemically to induce eosinophilia and within tissues to promote local chemotactic signals. Regulation of IL-5 and eotaxin levels within the lung by IL-4 and IL-13 allows Th2 cells to elegantly co-ordinate tissue and peripheral eosinophilia. Whilst the inhibition of either the IL-4/IL-13 or IL-5/eotaxin pathways resulted in the abolition of tissue eosinophils and AHR, only depletion of IL-5 and eotaxin concurrently results in marked attenuation of pulmonary inflammation. These data highlight the importance of targeting both IL-5 and CCR3 signalling systems for the resolution of inflammation and AHR associated with asthma.

Effect of Cefadroxil on Antigen-Induced Bronchial Hyperresponsiveness and Eosinophil Accumulation in Lung from Sensitized Guinea Pigs

The effect of a semi-synthetic cephalosporin, Cefadroxil, on antigen-induced bronchial hyperresponsiveness and eosinophil accumulation in lungs from sensitized guinea pigs was investigated and compared to the effects of Cetirizine and Ketotifen. When aerosol-sensitized guinea pigs were pretreated 1 h before the antigen challenge with Cefadroxil (100 mg/kg i.p.) a partial but significant inhibition of the bronchial hyperresponsiveness to aerosolized acetylcholine chloride was observed. Furthermore, the treatment of guinea pigs (115 mg/kg, per os) 24 and 1 h before ovalbumin challenge also significantly reduced bronchial hyperresponsiveness. In contrast, no significant inhibition was noted when the guinea pigs were treated by a single dose of Cefadroxil (115 mg/kg per os) 1 h before challenge. Pretreatment of the guinea pigs with Cetirizine (1 mg/kg per os) or Ketotifen (0.1 mg/kg per os) completely inhibited the antigen-induced bronchial hyperresponsiveness. Cefadroxil (100 mg/kg i.p.) slightly inhibited the accumulation of eosinophils in the peribronchial area induced by antigen challenge. In contrast, no significant reduction was noted when the guinea pigs were treated per os with Cefadroxil (115 mg/kg), Cetirizine (1 or 10 mg/kg) or Ketotifen (0.1 mg/kg). These results show that Cefadroxil is effective in reducing antigen-induced bronchial hyperresponsiveness, an effect independent of a reduction in the pulmonary inflammation, namely eosinophil accumulation in lung.